Significant Increase In Plasma Prolactin Research Articles

Effects of Vasoactive Intestinal Peptide on Prolactin Secretion in Three Species of Passerine Birds

Previous work on domesticated species has indicated that vasoactive intestinal peptide (VIP) is an important prolactin-releasing factor in these birds, but no comparative work in passerine birds has been reported. This study showed that iv injections of VIP (50–100 μg/kg body mass) result in a dramatic, but transitory, rise in plasma prolactin in Mexican jays (Aphelocoma ultramarina). Significant increases in prolactin were also observed following VIP injection in blue jays (Cyanocitta cristata) and zebra finches (Poephilla guttata). At the dosage we used, maximum levels of prolactin attained were slightly lower (Mexican jays) or very similar (blue jay and zebra finch) to the maximum prolactin levels observed in other, breeding birds of the same species. In zebra finches that initially had low prolactin, VIP injection resulted in a greater than 10-fold increase in prolactin within 10 min, but those individuals that already had elevated prolactin showed no further increase in response to VIP. Slow-release pellets of VIP implanted subcutaneously in Mexican jays and releasing 10 or 15 μg VIP/day (two or three pellets) produced a significant increase in plasma prolactin (78 and 92% rise, respectively) compared to birds with placebo pellets or with with one pellet releasing only 5 μg/day.

Changes in plasma prolactin and catecholamine metabolite levels following acute needle stick in children

Changes in plasma levels of prolactin (PRL), homovanillic acid (HVA), and 3-methoxy-4-hydroxyphenylglycol (MHPG) following insertion of an indwelling catheter into a forearm vein were assessed in 11 boys with attentiondeficit hyperactivity disorder. Results indicated decreases in plasma PRL and HVA, but not MHPG, from the time of needle stick until 105 min post-insertion. These data indicate a significant increase in plasma PRL and HVA in children following needle stick which gradually decreases over a 1.5–2-h period. These stress-induced changes indicate that values obtained immediately after needle insertion cannot be assumed to accurately reflect baseline levels.

Morphine-induced prolactin release precedes a down-regulation of prolactin receptors in the male rat choroid plexus and hypothalamus

In previous studies we provided evidence for changes in prolactin (PRL) receptor levels in the male rat brain after continuously infusing morphine using subcutanously implanted miniosmotic pumps. In this work we have studied the binding of PRL in the male rat brain following morphine administration by both subcutaneous (s.c.) and intracerebroventricular (i.c.v.) injections. The binding in the choroid plexus and the hypothalamus was measured using iodinated ovine PRL (oPRL) as a radiolabel. The results indicated that the density of the PRL-binding sites in the hypothalamus and the choroid plexus were significantly decreased 4 h and 24 h after s.c. injections, and also 30 min and 4 h after i.c.v. injections. However, no decrease in PRL-binding was observed 15 min after i.c.v. injection of morphine. The plasma levels of PRL were measured by radioimmunoassay (RIA) and were found to be significantly increased after 30 min and 4 h in all treated animals. Following i.c.v. injection a significant increase in plasma PRL was observed after just 15 min. It was suggested that the down-regulation in PRL binding to some extent at least resulted from receptor overstimulation caused by the morphine-induced elevation in the concentrations of the endogenous hormone.

Effects of hyperprolactinemia on plasma glucose and prolactin in rats exposed to ether stress

The present study was designed to characterize the effect of chronic hyperprolactinemia on plasma glucose and prolactin (PRL) during ether stress in male and female rats. Wistar rats of both sexes were divided into a hyperprolactinemic group (bearing pituitary grafts) and a control group (sham operated). They were exposed to ether during 10 min and had blood samples taken immediately before, and 5, 15, 40, and 70 min after ether exposure and assayed for glucose and PRL concentrations. Ether stress induced significant increase in plasma PRL of control rats at 5 min (male 171%, female 161%; P < 0.01), but only a mild PRL increase occured in grafted rats (male 66%, female 62%; P < 0.05). Control male rats sustained elevated plasma PRL longer than females. There was a marked elevation of glucose levels at 5 min ( P < 0.01) which peaked at 15 min in all groups. Grafted rats had glucose levels significantly above control at baseline (female 15%, P < 0.05) and at 40 min (male 25%, female 29%; P < 0.05). It is concluded that ether-induced PRL release produced a rapid and transient response, more intense in males than in females and which was impaired by previous hyperprolactinemia (pituitary grafts). There was an acute hyperglycemic response, plasma glucose being increased in grafted rats, supporting the hypothesis of a hyperglycemic effect of PRL.

Evidence that amplification of norepinephrine-induced LH release by morphine is indirectly due to suppression of tuberoinfundibular dopamine secretion

We previously observed that morphine markedly amplifies LH secretion following intracerebroventricular (i.c.v.) norepinehrine (NE) infusions. Based on additional evidence, we hypothesized that perhaps these morphine effects were due to suppression of tuberoinfundibular dopamine (TIDA) secretion thus allowing NE to evoke a greater release of LHRH from axon terminals in the median eminence than would otherwise occur. In the present studies, we examined whether apomorphine (a DA receptor agonist) would suppress and haloperidol (a DA receptor antagonist) would mimic these enhancing effects of morphine on NE-induced LH secretion. Estrogen-treated ovariectomized rats were used in these studies. NE, when infused i.c.v. (45 μg) evoked a modest increase in plasma LH(1.1 ± 0.2to2.2 ± 0.2ng/ml) within 15 min. When morphine sulfate (10 mg/kc s.c.) was given 15 min prior to NE, LH peak values of11 ± 2ng/ml were obtained by 60 min. Treatment of rats with apomorphine (1.5 mg/kg s.c.) at −15 min, morphine at 0 min and i.c.v. NE at 15 min resulted in a significant blunting of morphine's effect on NE-induced LH release. Moreover, in all morphine-treated rats, plasma prolactin (PRL) increased significantly within 10 min, peaked at 30 min and declined towards basal values by 90 min. Apomorphine completely blocked this morphine effect of PRL release. Haloperidol (HAL; 2.5 mg/kg s.c.) treatment had no effect on basal LH release but resulted in a significant increase in PRL which remained elevated up to 180 min. When HAL was given at 0 min and NE was infused i.c.v. at 15 min, a rapid, progressive and highly significant temporal increase in LH secretion occurred with peak values of20.4 ± 4ng/ml being reached by 90 min. Since our other recent studies have shown that i.c.v. DA infusions neither amplify nor suppress NE-induced LH release nor do they affect basal LH levels when given alone, we could not attribute morphine's action on NE release to alterations in A15 or A14 DA neuronal activity nor to increases in hypothalamic incertohypothalamic (A13) DA secretion. Rather, the suppression of TIDA (A12) neuronal activity or blockade of DA receptors by morphine or HAL, respectively, suggest that amplification of NE-induced LH release may be due to the suppression of inhibitory DA influences on the release of LHRH from axon terminals within the median eminence. The implications of these opiate actions on preovulatory LH surges are discussed.

Effects of serotonergic agents on plasma prolactin levels in pyridoxine-deficient adult male rats

Plasma concentration of prolactin was significantly reduced in pyridoxine-deficient as compared to control (pyridoxine-supplemented) adult male rats. Administration of pyridoxine to deficient rats resulted in a significant increase in plasma prolactin. The reduction in plasma prolactin in pyridoxine-deficient rats corresponded with the significantly reduced hypothalamic contents of pyridoxal phosphate and serotonin in pyridoxine-deficient rats. Plasma prolactin concentrations were also measured in response to serotonergic agents in both groups of rats. The administration of the 5HT1A agonist (8-hydroxy 2-n-dipropylamino tetralin) resulted in a significant increase in plasma prolactin and that of the specific 5HT1A antagonist spiroxatrine had the opposite effect. The results suggest that the hypothalamic serotonergic regulation of prolactin release is impaired in pyridoxine deficiency.

Small Dose of Domperidone Potentiated the Effects of TRH and Serotonin on Prolactin Release in Ovariectomized, Estrogen-Treated Rats

A transient antagonism of the dopaminergic action by using a dopamine antagonist, domperidone, plus a dopamine agonist, CB154, has been shown to potentiate the effect of thyrotropin-releasing hormone (TRH) on prolactin (PRL) secretion. In order to test whether the serotonin (5-HT)-induced PRL secretion can also be enhanced in a similar way, we used 5-HT instead of TRH in our first experiment. We found that the dose of domperidone used (10 micrograms/rat) seems to be excessive since it induced a marked and substantial increase in PRL release and the use of CB154 further masked the action of 5-HT. We used a smaller dose of domperidone (1 microgram/rat) without the CB154 and found that it induced a moderate amount of PRL release which lasted for over 1 h. Given TRH (1 microgram/rat) or 5-HT (0.3 mg/rat) 1 h later resulted in a significant increase in plasma PRL which was much higher than that induced by TRH or 5-HT alone. The potentiating effect of domperidone was even more significant for the 5-HT- than the TRH-stimulated PRL secretion. Pretreatment with 5-HT or vasoactive intestinal polypeptide (10 micrograms/rat) were without any effect in potentiating the action of TRH. In conclusion, antagonizing the dopamine action appears to enhance the stimulatory effect of TRH and 5-HT on PRL secretion.

Effect of various catecholamine antagonists on prolactin secretion in conscious male rabbits.

To clarify physiological roles of catecholaminergic systems in the control of rabbit prolactin (PRL) release, the effect of various catecholamine receptor antagonists on plasma PRL levels was examined in conscious, freely moving male rabbits. An intravenous (iv) injection of yohimbin (2.5 mg/kg body wt), an alpha 2-adrenoreceptor antagonist, but not prazosin (2 mg/kg body wt), an alpha 1-adrenergic receptor antagonist, resulted in a significant elevation of plasma PRL. Conversely, propranolol (2.5 mg/kg body wt, iv), a nonselective beta-adrenoreceptor antagonist, and metoprolol (2.6 mg/kg body wt, iv), a beta 1-adrenergic antagonist, slightly but significantly suppressed basal levels of plasma PRL. On the other hand, haloperidol (0.5 mg/kg body wt, iv), pimozide (0.3 mg/kg body wt, iv), sulpiride (5 mg/kg body wt, iv), chlorpromazine (3 mg/kg body wt, iv), and YM-09151-2 (0.2 mg/kg body wt, iv), all dopamine receptor antagonists caused a significant increase in plasma PRL. These results suggest that dopaminergic and alpha 2-adrenergic mechanisms exert a tonic inhibitory role and beta-adrenergic mechanisms, probably beta 1, a tonic stimulatory role in the regulation of PRL release in the rabbit.

Hypothalamic monoaminergic activity and pituitary function in male rats with estrogen-induced pituitary hyperplasia.

The mechanism by which estrogen enhances prolactin (PRL) secretion and induces hyperplasia of lactotrophs is not defined clearly. The objective of this study was to examine hypothalamic monoaminergic PRL regulatory systems and pituitary hormone secretion in the early and later stages of estrogen-induced hyperprolactinemia and pituitary hyperplasia. Dopamine (DA) and serotonin (5-HT) turnover were determined in microdissected brain regions 3 and 30 days after a single subcutaneous dose of estradiol (2 mg) to male ACI rats. Plasma samples were collected in animals with indwelling intra-atrial cannulae. 3 days after estrogen there was a significant increase in plasma PRL, pituitary PRL and growth hormone (GH), and DA turnover in the median eminence and arcuate nucleus. Plasma concentrations and pituitary content of PRL increased at 30 days. The responsiveness of PRL to thyrotropin-releasing hormone (TRH) was enhanced at both times. Concentrations of DA decreased considerably in the median eminence and arcuate nucleus by 30 days, and turnover decreased in the median eminence. 5-HT turnover was not affected in the early stages of hyperprolactinemia. Plasma GH increased and TSH was unchanged, even though pituitary content of both hormones decreased at 30 days. Estrogen had no effect on plasma corticosterone. These findings support the hypothesis that estrogen induces pituitary hyperplasia by antagonizing DA inhibition of PRL-secreting cells and by enhancing their responsiveness to TRH.

Responses of prolactin and growth hormone to L-tryptophan infusion: Effects in normal subjects and schizophrenic patients receiving neuroleptics

Intravenous infusion of L-tryptophan (LTP) in 18 normal subjects produced a significant increase in plasma prolactin (PRL), growth hormone (GH), and self-ratings of drowsiness. There was no correlation between the PRL and GH responses, or between the hormonal responses and drowsiness. Saline infusion did not result in endocrine or psychological changes. The effect of LTP on both PRL and GH was dose-related in that LTP 7.5 g produced greater endocrine responses than 5.0 g. It was not significantly decreased by cyproheptadine, a 5-HT receptor antagonist. Schizophrenic patients receiving neuroleptics had increased PRL response to LTP, possibly because of the drug-induced disinhibition of PRL release. Their GH response to LTP was markedly decreased. The mechanism of this effect requires further investigation.

Prolactin and luteinizing hormone levels of prelaying, laying and postlaying turkey hens following central administration of serotonin and peripheral administration of quipazine maleate

The influence of serotonin (5-HT) on plasma prolactin and LH levels in female turkeys was studied by systemic injection of quipazine maleate, at 5-HT agonist, or by cerebro-ventricular injection of 5-HT itself. Within 30 min after injection, quipazine maleate (20 mg administered i.p.) elicited a significant increase in plasma prolactin in hens approaching sexual maturity as well as in laying hens. A 5-mg dose. had no effect on prolactin levels of either prelaying or laying hens. Intraventricular injection of 5 and 25 μg of 5-HT caused an increase in plasma prolactin of prelaying hens. A 5-μg dose of 5-HT was also effective in increasing prolactin levels in laying hens and in hens that had stopped laying due to ventricular cannula implantation. Neither quipazine maleate nor intraventricularly injected 5-HT had an effect on LH levels in any experiment.

The effect of short and skeleton long photoperiods on the plasma concentrations of prolactin and cortisol in sheep.

Suffolk-cross lambs, aged eight weeks, were exposed to either short photoperiods (8L : 16D, SP; 7 castrated males and 6 females) or skeleton long photoperiods (7L : 10D : 1L : 6D, SLP; 6 castrated males and 7 females). They were fed individually on a complete pelleted diet at 70 g/kg live weight 0.75/day. Blood samples were taken monthly by jugular puncture for three months and, after 39 days on experiment, jugular catheters were inserted for frequent sampling over a 24 h period. The samples were assayed for prolactin using radioimmunoassay and for cortisol by competitive protein binding. SLP caused a large and significant increase in plasma prolactin throughout the experiment, with no effect on sex. During the 24 h period there were consistent peaks of prolactin at the start of both dark phases under SLP, with lower levels around the start of both light phases; under SP, prolactin tended to be higher in the middle of the light phase and the middle of the dark phase than at other times. Considerable hourly fluctuations were observed in cortisol levels but an obvious 24 h rhythm was not. Mean levels were, however, significantly higher under SP (38.3 nmol/l) than under SLP (26.8 nmol/l).

Evidence for a Role of Prolactin in Prostate and Seminal Vesicle Growth in Immature Male Rats

To determine if prolactin secreted endogenously by anterior pituitary grafts could augment male accessory organ weights, single anterior pituitary grafts were placed under the kidney capsule of male rats, whereas control animals received a graft of muscle. Three weeks after transplantation, the animals were sacrificed by decapitation and a significant increase in plasma prolactin was observed, which was accompanied by a highly significant increase in the weights of seminal vesicles, ventral and dorsal prostates, and adrenals. To determine the importance of testicular steroids in the response, animals were castrated. The increases in prolactin, seminal vesicle and ventral and dorsal prostate weights still occurred whether or not a small dose of testosterone replacement therapy was employed. In the presence of the pituitary graft, adrenal weight usually increased in these animals as well. To rule out a requirement for adrenal steroids in the response, adrenalectomized-castrate animals were also studied, and the increases in prolactin and prostate weights still occurred although there was no significant increase in the size of the seminal vesicles. To rule out the participation of other pituitary hormones, pituitary grafts were also placed in hypophysectomized animals, and in these animals, there was also a significant increase in prolactin, accessory sex organ and testicular weights, but the adrenals did not increase in size. The grafts failed to alter gonadotropin titers in any experiment. It is concluded that single anterior pituitary grafts are capable of secreting sufficient prolactin to increase the size of the sex accessories and sometimes the testes and adrenals of the rat. Furthermore, the effects on the male sex accessory organs were demonstrable in the absence of testicular or both testicular and adrenal steroids. The data suggest that prolactin may play a physiological role in the growth of the testes, adrenals and sex accessories.

The influence of estrogen on plasma prolactin levels induced by Thyrotrophin Releasing Hormone (TRH), clonidine and serotonin in ovariectomized rats

Prolactin levels were determined in the plasma of ovariectomized and ovariectomized estrogen treated rats by RIA following intraarterial injection of TRH, (1 and 10 μg/rat), clonidine (5 mg/kg) and serotonin (10 mg/kg). In ovariectomized rats, TRH had no effect on plasma prolactin whereas serotonin and clonidine induced slight and moderate increases respectively. In contrast, TRH induced a significant increase in plasma prolactin in estrogen-treated rats while the effects of the other two agents were enhanced only slightly (clonidine) or very markedly (serotonin). These results indicate that the prolactin-releasing activity of TRH is dependent on estrogen and that estrogen differentially affects noradrenergic and serotonergic components of the neuroendocrine mechanism that controls prolactin. It is also suggested that clonidine and serotonin probably do not increase plasma prolactin by releasing endogenous TRH.